Tuesday, August 25, 2015

Starchy stable isotopes? I don't think so!

“…stable isotope analyses indicate a mainly carnivorous diet for Neanderthals; a wider range of isotopic values have been observed in contemporary Middle Pleistocene H. sapiens (Richards and Trinkaus 2009), indicating that considerable differences in the levels of starch consumption existed between these two species.”

Now, if you read this I think you might be led to believe that stable isotope analysis indicates that Neanderthals were carnivores and H sapiens ate a different amount of starch to a carnivore. I feel the implication of this sentence is that H sapiens ate "more-than-zero starch" during the Middle Pleistocene.

You would believe wrongly. Did you check the reference? No? Naughty. Richards and Trinkaus (2009) actually say this:

“As the method only measures protein intake, many low-protein foods that may have been important to the diet (i.e., high caloric foods like honey, underground storage organs, and essential mineral and vitamin rich plant foods) are simply invisible to this method.”

The data do not deny starchivory. But the data equally do not in any way support its occurrence. Starch, fruit and honey are invisible on stable isotope analysis. This is a gross mis-citation of Richards and Trinkaus by Hardy et al. Never believe stuff like this without checking the refs. Easy when it is a freebie in PLOS. What do Richards and Trinkaus actually say about diets of carnivorous Neanderthals vs H sapiens? Try this:

“There are now enough isotopic data to see patterns in the data, and they show that the Neanderthals and early modern humans had similar dietary adaptations, obtaining most of their dietary protein from animals, although some of the early modern humans obtained significant amounts of their protein from aquatic, and not just terrestrial, sources.”

You can tell H sapiens ate fish because aquatic food chains are long. The longer the food chain the greater the effect visible in stable nitrogen isotopes. They make fish eating carnivores look like hyper-carnivores. That's how they show up in the paper. Had humans eaten any significant amount of protein rich plants (hazel nuts get cited as a possibility) it would show a lower stable nitrogen ratio. There is no evidence for this.

Did early humans consume starch to grow their brain size? Stop laughing! No one knows, certainly to the point where a starchivorous paper has to mis-cite a completely non-supportive paper as being actually supportive of their rubbish hypothesis.

I love it.

Did you hear the one about Jennie Brand-Miller? Passthecream linked to this gem in the comments of the last post. Some things are just too funny not to share. Have a giggle. J B-M is second author on the starch-is-needed-to-grow-brains paper...

@Raphi: AMY1 copy number increase also evolved in dogs in the same period. Both wolves and chimps have two copies, both dogs and people vary in number. So there's pretty clearly severed pressure to adapt to a high-carb diet. The question, of course, is why?

It turns out that the bacteria that turn starch into tooth-decaying acids use salivary amylase to do the conversion: they can't do it themselves.

There's exactly one (that I could find) study that looks into the effect of multiple AMY1 copies on dental health. They found that people with multiple copies have lower rates of caries.

If this is correct it means that the evolutionary pressure is a defensive one: to protect the teeth from rotting out.

Sort of speaks against the health benfits of starch... ;)

The other interesting thing I've learned is that, while we evolved from frugivores who had a high sucrose diet, we do not have salivary sucrase enzyme to break it down. Salivary sucrase is a sign of bacterial activity. So it's not a great argument to make to say salivary amylase is needed for digesting starch.

It's an interesting question why we have salivary amylase then in the first place, let alone why wolves have it.

Miki, I've enjoyed reading your blog and listening to the AHS presentation immensely (I never listen to podcasts!). There are so many problems when anyone falls in love with an idea. The cooked starchers clearly have problems with reality and the omega 3 and DHA-ers have some ridiculous ideas on board, some quite funny. I like your self questioning and methodical approach through energetics. Thanks for putting your ideas out there.

Would you mind linking to that paper looking at AMY1's effects on dental health? raphi.inter@gmail.com. Thanks.

"Both wolves and chimps have two copies, both dogs and people vary in number" ==> You make a good point that the adaptation, so far, appears to have been more of a defensive move rather than an 'embracing' one.

"It's an interesting question why we have salivary amylase then in the first place, let alone why wolves have it." ==> I don't know what the what the timeline says about dog domestication & their AMY2B (pancreatic amylase) CNV increase but...could they have adapted alongside us to make the best of our scraps? But then why no AMY1?

What we DO know about AMY1 is that it doesn't help our metabolism deal with carbohydrate better since you're as likely to be obese whether you have 4 or 14 copies. Seems like this riddle is going to be a slow process of eliminating hypothesized functions...

Seems to be a lot of money up for grabs at the moment - Rory Robertson and Anthony Colpo have thousands of our (currently pathetic) $AUD on offer, albeit for different things. Coincidentally, they also both have thoughts on offer re the Australian Paradox.

I wonder if Rory would have gotten any better response from Sydney Uni if he'd gone "Full-Colpo" on them.

It turns out that the bacteria that turn starch into tooth-decaying acids use salivary amylase to do the conversion: they can't do it themselves.

If this is correct it means that the evolutionary pressure is a defensive one: to protect the teeth from rotting out.

I didn't get the jump to the conclusion here. If bacteria need salivary amylases to convert starch to acid, then wouldn't more amylase produce more acid? If so, how is that protective? Seems it would be more damaging.

Instant hypothesis, just add water and research : grains contain amylase inhibiting enzymes, greater amounts of amylase would counter the effect of greater (relative) inputs of seed based food. This is a zero sum game for calorie intake but gives an advantage in terms of novel food choices.

Stipetic: "I didn't get the jump to the conclusion here. If bacteria need salivary amylases to convert starch to acid, then wouldn't more amylase produce more acid? If so, how is that protective? Seems it would be more damaging."

Unless more salivary amylase prevents the bacteria from getting the starch.

If it's digested into glucose before the bacteria can do it, it would prevent them from producing the acids that actually rot the teeth. Not a 100% solution, but an improvement.

Would you mind linking to that paper looking at AMY1's effects on dental health? raphi.inter@gmail.com. Thanks.

Will do, when I can find it again: it wasn't a great study: it was from Iran, but it was the only one I could find. I don't seem to have saved the link or the study...

"...could they have adapted alongside us to make the best of our scraps?...

Yes, I think that's exactly what happened.

"What we DO know about AMY1 is that it doesn't help our metabolism deal with carbohydrate better since you're as likely to be obese whether you have 4 or 14 copies...."

I can give you this link:

"The chance of being obese for people with less than four copies of the AMY1 gene was approximately eight times higher than in those with more than nine copies of this gene. The researchers estimated that with every additional copy of the salivary amylase gene there was approximately a 20 per cent decrease in the odds of becoming obese."

http://www.sciencedaily.com/releases/2014/03/140330151318.htm

That's a huge signal for an epidemiological signal, btw. On the order of the signal that smoking tobacco causes lung cancer—indicative of a likely strong causal relationship.

The cause appears to be that people with more AMY1 copies detect the glucose earlier, secrete insulin earlier, and therefore can secrete less insulin to deal with the bolus—that's another paper that I don't have time for find the link for right now...

""It's an interesting question why we have salivary amylase then in the first place, let alone why wolves have it." ==> I don't know what the what the timeline says about dog domestication & their AMY2B (pancreatic amylase) CNV increase but...could they have adapted alongside us to make the best of our scraps? But then why no AMY1?"

"...These observations are interpreted to suggest that [high-amylase] individuals may be better adapted to ingest starches, whereas [low-amylase] individuals may be at greater risk for insulin resistance and diabetes if chronically ingesting starch-rich diets."

http://www.nature.com/doifinder/10.1038/ng.3340 Usher et al. 2015 'Structural forms of the human amylase locus and their relationships to SNPs, haplotypes and obesity' ==> 3 cohorts for a total of 51,535 Estonians.

1) "Obese and lean individuals show indistinguishable distributions of AMY1 copy number (P > 0.05)...We had >99% power to detect (at nominal significance) effects as strong as those reported. However, we did not observe even a nominal association between obesity and the copy number of any amylase gene (P = 0.70 for AMY1)"2) The previous strong association you cite were due to "low-resolution, poorly clustering molecular data conceal technical effects that can create the false impression of strong association"3) Authors believe that the "the difference from the reported observation likely comes from our use of higher-resolution approaches for both molecular and computational analysis"

Point 3 has to do with read-depths relating to sequence coverage. The latter is the number of times a nucleotide is read during the sequencing process [Formula: N x (L x G)] N = # of reads, L = average length of reads, G = length of original genome.>x7 = deep ... >x100 = ultra deep.

The association (AMY1-obesity) has been pretty much definitively put to rest in my mind.

"Conclusion: Generally it can be concluded that low levels of alpha-amylase may promote early childhood caries. On the other hand, dental caries may subsequently reduce the level of salivary alpha-amylase. This vicious cycle may promote and then accelerate caries formation among susceptible people with low level of salivary alpha-amylase."

"Effect of alpha amylase on early childhood caries"PDF: http://ojs.fosjc.unesp.br/index.php/cob/article/viewFile/873/795

Thanks for responding, Tucker. I'm still trying to understand. You said,

If it's digested into glucose before the bacteria can do it, it would prevent them from producing the acids that actually rot the teeth. Not a 100% solution, but an improvement.

I thought bacteria use glucose to make acid (your original post seems to imply bacteria can't utilize starch directly, that it needs amylase to convert it to a usuable form; glucose). If so, more amylase should produce more sugar, which bacteria would use to produce more acid, which would then lead to more caries (and this process would likely grow more bacteria too and lead to a vicious cycle). Inversely, less amylase would lead to more starch going unprocessed directly to the stomach, leaving less glucose for the bacteria to turn into acid--fewer amylase copies = beneficial (less caries). But that's not what you are saying and not what's been shown empirically (Iranian paper).

However, if bacteria utilise starch directly, then the availability of usable substrate to bacteria is inverse and the argument works.

The evolutionary pressure argument doesn't seem to work if bacteria use glucose directly. Sweets cause caries, right? In essense, I'm not seeing how the number of copies appears to be defensive in order to protect teeth from rotting. Unless it does so by some other mechanism. Did I missunderstand or misinterpreted? Cheers.

I expected that AMY1 multiple copies would produce more caries, as you describe. We have one not-great study showing the opposite. I was trying to come up with an explanation as to why that might be the case. Pure speculation on my part, in other words.

S. mutans uses glucose, or, given salivary amylase, it uses that to digest starch, releasing lactic acid. My thought was that a higher amylase enzyme level may reduce the time the starch is in the mouth, thereby reducing the amount available to S. mutans for acid production.

The other major characteristic of starch that causes caries is stickiness: likeliness that starch is stuck to the teeth, where S. mutans lives. Less sticky starch like rice is less cariogenic.

So reducing that sticky starch to glucose and getting it off the teeth as fast as poassible would reduce the amount that S. mutans could convert to acid.

But again, it's pure speculation, as I was hoping to explain an effect contrary to what I was expecting to see.

What an odd story Matesz is. I wonder if he feels bad about charging people for dietary consultations when he was "paleo." Did they all get refunds? Give him some more time, and he'll be praising Ray Peat.

Since you mentioned Matesz, I thought I'd also check out Guyenet, who of course is also proud of the recent low fat win. He seems to support statin use now, and has an anti-meat tone, though, to be fair, it isn't so aggressive (yet?).

What do other seed eating, non-ruminant animals do about starch, birds for instance?

Where I live we have a big problem with sparrows as an invasive species. These are thought to be another of the 'diseases' of civilisation, following the neolithic crops across from the middle east until they have almost come back full circle around the planet.

Zombie w/o bwains... Non-living proof of the shrinking human brain size! Stan, these people always make me think go JK's ideas about the slave temperament and a carb based nutrition. Intelligence is not required, contribution to the hive is what matters. What intelligence remains is used to claw up the carb society pyramid.

Rats and mice are seed based creatures but maybe they don't live long enough to get tooth decay? I don't know how they deal with agglutenins etc. but I guess they must have specific enzymes and digestive processes to handle them. I had a thought this afternoon that the high (10%) Western European prevalence of haemochromatosis might be a useful mutation wrt a diet heavy in grains and legumes.

Probably I'm wrong about rat diets there; one thing I remember about uncovering rats 'nests' in the garden when I was young was that were huge piles of almond and other stone fruit seeds from which the kernels had been eaten and just as many empty shells of garden snails. That looks like a high fat/high protein diet.

About Me

I am Petro Dobromylskyj, always known as Peter. I'm a vet, trained at the RVC, London University. I was fortunate enough to intercalate a BSc degree in physiology in to my veterinary degree. I was even more fortunate to study under Patrick Wall at UCH, who set me on course to become a veterinary anaesthetist, mostly working on acute pain control. That led to the Certificate then Diploma in Veterinary Anaesthesia and enough publications to allow me to enter the European College of Veterinary Anaesthesia and Analgesia as a de facto founding member. Anaesthesia teaches you a lot. Basic science is combined with the occasional need to act rapidly. Wrong decisions can reward you with catastrophe in seconds. Thinking is mandatory.
I stumbled on to nutrition completely by accident. Once you have been taught to think, it's hard to stop. I think about lots of things. These are some of them.

Organisation (or lack of it)!

The "labels" function on this blog has been used to function as an index and I've tended to group similar subjects together by using labels starting with identical text. If they're numbered within a similar label, start with (1). The archive is predominantly to show the posts I've put up in the last month, if people want to keep track of recent goings on. I might change it to the previous week if I ever get to time to put up enough posts in a week to justify it. That seems to be the best I can do within the limits of this blogging software!